Myocardial infarction

4,692 views 31 slides Mar 06, 2021
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About This Presentation

A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck or jaw


Slide Content

Treatment of Acute Myocardial Infarction

INTRODUCTION Prompt recognition is the key Earliest reperfusion gives maximum benefit First 60 minutes is called golden period Primary PCI vs Thrombolysis has almost same result when done in 1 st hour

Higher the TIMI flow lesser the mortality Irrespective the strategy to open the occluded artery, a good blood flow at the level of capillary is must to ensure better survival outcome.

Universal 4 th D efinition to classify ACS ,2020

4 th UNIVERSAL DEFINITION MI Chest pain: Typical:(3/3) Atypical :<3 ECG : Every 10 minutes till diagnosis Biomarker :Serial if initial negative ECHO is supportive

UNIVERSAL 4 TH DEFINITION of MI ,2020 Type 1: Plaque rupture – Thrombus formation – Lumen occlusion Type 2: There is no base line atheromatous plaque but imbalance between supply and demand causes ischemia. coronary dissection vasospasm Embolism microvascular dysfunction Type 3 : MI resulting in death when biomarker values are unavailable Type 4a: MI during Type 4b: Stent Thrombosis causing MI Type 5: CABG graft occlusion causing MI

WHEN TO SUSPECT ACUTE MI CHEST PAIN SOB SYNCOPE SUDDEN CARDIAC ARREST

ECG: Within 10 minutes After First Contact ST-elevation/new LBBB NSTEMI unstable angina ST-depression, T wave inversions, or transient ST-elevation Nondiagnostic :Follow with serial ECG

12 LEAD ECG STEMI ST segment elevations ≥1 mm (0.1 mV) in two anatomically contiguous leads or ≥2 mm (0.2 mV) in leads V2 and V3 New LBBB NSTEMI/USA ST segment depressions or deep T wave inversions without Q waves

TIMELINE OF ST/T CHANGES IN STEMI

STEMI New ST-segment elevation at the J-point in two contiguous leads with the cut-points: ≥0.1 mV in all leads other than leads V2-V3 V2-V3: ≥2 mm in men ≥40 years ≥2.5 mm in men <40 years ≥1.5 mm in women regardless of age

NSTEMI New horizontal or down sloping ST-depression ≥0.5 mm in two contiguous leads and/or T inversion >1 mm in two contiguous leads with prominent R wave or R/S ratio >1

Left bundle branch block ST-depression of at least 1 mm in leads V1, V2, or V3 or in leads II, III, or aVF, with elevation of at least 1 mm in lead V5 Extremely discordant ST changes (changes in the opposite direction of the major QRS vector of >5 mm) were also reported to be suggestive of MI

Nondiagnostic initial ECG Wait and watch

Old Myocardial Infarction in the absence of left bundle branch block or left ventricular hypertrophy Any Q wave in leads V2 to V3 ≥0.02 sec or QS complex in V2 and V3; Q wave ≥0.03 sec and ≥0.1 mV deep or QS complex in leads I, II, aVL, aVF; or V4 to V6 in any two leads of a contiguous lead grouping (I, aVL; V1 to V6; II, III, aVF) R wave ≥0.04 sec in V1 to V2 and R/S ≥1 with a concordant positive T wave in the absence of a conduction defect.

Findings on the ECG depend upon Duration – Hyperacute, acute, evolving, or chronic Size – Amount of myocardium affected Location – Anterior, lateral, inferior-posterior, or right ventricle

Troponin  Serial ECG is key :at first contact ,at 3hour ,at 6hour Quantitive : hS-Tp =00-0.02nano gram /ml Kit test (Qualitive ):>40 nano gram /ml Routine quantitative :>give the value if it is >40 nano gram /ml (ROCHE’s Lab)

IMAGING ECHO MRI SPECT

CT CORONARY ANGIO IN ACUTE MI Only when in the presentation is quite atypical To rule out CAD

TREATMENT PRINCIPLE Diagnosis of ACS : Universal 4 th Definition of MI Relief from Angina : Sublingual Nitroglycerin (5mg)/ Morphine / Pentazocine Monitoring vitals Reperfusion strategy :TLT VS PCI Antiplatelet therapy : Ecosprin is must and others Statin therapy : High dose Anticoagulation ( UFH,LMWH,Fondaparinux ) Beta blocker therapy, ACEI: Depending upon BP

Initial Management Care for ABC O xygen if O 2  saturation < 92% Treat VT/VF according to ACLS protocols Aspirin 325 mg (non-enteric coated) to be chewed

Thrombolysis in MI

Contraindication for TLT Absolute :IC bleed Relative :Pregnancy ,HTN

thrombolytic regimens for acute ST elevation myocardial infarction

Give oral antiplatelet therapy (in addition to aspirin) to all patients: 1.  Patients treated with fibrinolytic therapy:  Give clopidogrel loading dose 300 mg if age 75 years or less; if age over 75 years, give loading dose of 75 mg 2.  Patients treated with no reperfusion therapy:  Give ticagrelor loading dose 180 mg. 3.  Patients treated with primary PCI:  Give ticagrelor loading dose of 180 mg or prasugrel loading dose of 60 mg (if no contraindications: prior stroke or TIA, or relative contraindications for prasugrel such as those age 75 years or older, weight less than 60 kg). For patients at high risk of bleeding or those for whom prasugrel or ticagrelor cannot be used, we give clopidogrel 600 mg. Give anticoagulant therapy to all patients 1.  For patients treated with primary PCI,  we prefer UFH to bivalirudin. Dosing of UFH:  An initial IV bolus of 50 to 70 units/kg up to a maximum of 5000 units. Additional heparin may be given in the catheterization laboratory based on the results of ACT monitoring. Dosing of bivalirudin:  Initial bolus of 0.75 mg/kg IV followed by IV infusion of 1.75 mg/kg per hour; can be discontinued after PCI.   For patients treated with fibrinolysis,  we prefer enoxaparin for patients not at high bleeding risk or fondaparinux for those at high bleeding risk. For those patients in whom PCI is possible or likely after fibrinolytic therapy, UFH is reasonable.

Dosing of enoxaparin Patients <75 years: Loading dose of 30 mg IV bolus followed by 1 mg/kg subcutaneously every 12 hours; maximum of 100 mg for the first two subcutaneous doses. The first subcutaneous dose should be administered with the IV bolus. Dose adjustment for renal impairment ( CrCl <30 mL/minute)*: Loading dose of 30 mg IV followed by 1 mg/kg subcutaneously every 24 hours. The first subcutaneous dose should be administered with the IV bolus. Patients ≥75 years: No IV loading dose. Administer 0.75 mg/kg subcutaneously every 12 hours; maximum of 75 mg for the first two doses. Dose adjustment for renal impairment ( CrCl <30 mL/minute)*: No IV loading dose. Administer 1 mg/kg subcutaneously every 24 hours. Supplemental IV bolus dose for patients who will receive PCI after >1 dose of therapeutic enoxaparin: 0.3 mg/kg if last enoxaparin dose was given 8 to 12 hours earlier; no supplemental IV dose if last enoxaparin dose was within 8 hours; use UFH if last enoxaparin dose was more than 12 hours ago. Dosing of UFH:  IV bolus of 60 to 100 units/kg to a maximum of 4000 units, followed by an IV infusion of 12 units/kg per hour (maximum 1000 units per hour) adjusted to achieve a goal aPTT of approximately 50 to 70 seconds (1.5 to 2 times control). Dosing of fondaparinux:  2.5 mg intravenously, followed by 2.5 mg subcutaneously every 24 hours. This drug should be avoided in CrCl <30 mL/minute.

For patients not receiving reperfusion therapy,  we use enoxaparin or UFH. Dosing of enoxaparin:  Dose same as for patients treated with fibrinolysis (refer to section 2 above). Dosing of UFH:  IV bolus of 50 to 70 units/kg to a maximum of 5000 units, followed by an IV infusion of 12 units/kg per hour adjusted to achieve a goal aPTT of approximately 50 to 70 seconds (1.5 to 2 times control)

Acute management of unstable angina or non-STEMI: Give antiplatelet therapy (in addition to aspirin) to all patients: Patients not treated with an invasive approach:  Give ticagrelor loading dose 180 mg.   For patients managed with an invasive approach:  Give ticagrelor loading dose of 180 mg at presentation. Prasugrel loading dose of 60 mg may be used as an alternative if given after diagnostic coronary angiography.

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